Myocardial Infarction (MI) or Acute Myocardial Infarction (AMI) is defined as necrosis of cardiomyocytes due to the temporary or permanent ischemia in the areas of one or more coronary arteries. The MI or AMI is the leading cause of death in industrialized countries, in France with 120,000 cases reported in 2014, including 18 000 deaths. The generalization of coronary angioplasty, fibrinolytic and antithrombotic treatments resulted in a significant decline in mortality at one month, around 5% in large randomized trials [1]. But these encouraging results should not obscure the growing incidence of post-infarction heart failure. Indeed, the MI or AMI can result in a deleterious remodeling involving left ventricular dilation decreased heart contractile function exposure to the risk of heart failure.
It is currently accepted that part of myocardial damage during coronary occlusion are not directly related to tissue hypoxia. Transient or permanent myocardial ischemia induces the recruitment of inflammatory cells of the innate and adaptive immunity in the myocardium [2]. Several studies have shown that neutrophils and monocytes involved in conventional deleterious remodeling by producing pro-inflammatory cytokines, oxygen free radicals and matrix proteases. [3] There are over thirty years, Romson et al. had already reported the pathogenic role of neutrophils in an infarction model in dogs showing a decrease in the size of the infarct in the depletion of neutrophils [4].
The role of lymphocytes has been explored only recently. In their laboratory, inventors have shown that mature B2 lymphocytes play a deleterious role in postischemic ventricular remodeling in particular producing a CCL-7 chemokine that promotes the recruitment of monocytes from the bone marrow into the blood and then to the myocardium ischemic [5]. The overall role of CD4 T cells remains controversial. It has been shown that T lymphocyte subpopulation called regulatory CD4+Foxp3+protects against postischemic remodeling through the production of anti-inflammatory mediators such as IL-10 and TGF-β [6]. Similarly, the role of CD8 T cells remains also controversial. The role of cytotoxic CD8 T cells has never been studied in vivo. One study reported that the in vitro CD8 T cells may induce apoptosis in rat cardiomyocytes [7] but a recent study (Curato et al 2010) suggests that a subtype of CD8 T cells is increased after acute MI and has a cardioprotective role during MI. Thus, there is a need to understand clearly the role of CD8 T cells during MI.